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Flashcards in Acut kidney injury Deck (50)
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31

What are the usual causes of acute interstitial nephritis? Presentation? Lab abnormalities?

- most cases related to med use
- also caused by bacterial, viral or fungal infections of the kidney
presentation- 1/3 of time hx of maculopapular rash, fever, and arthralgias
labs- EOSINOPHILS in urine

32

What is the most common type of acute intrinsic renal injury? 3 main causes?

ATN
- 3 main causes:
ischemia, sepsis, and nephrotoxic drugs

33

When does ATN occur?

- when tubules fail to fxn
- failure to reabsorb BUN so BUN/Cr ratio should be less than 10:1
- failure to reabsorb Na and water = lead to elevated urine Na+ (greater than 20) and low urine SG and osmolality (less than 450)
- cell sloughing causes urine to be positive for sediment = MUDDY BROWN casts (granular), renal tubular epithelial cells and epithelial cell casts

34

Why would ATN be secondary to ischemia?

- tubular damage from site of low perfusion
- inadequate GFR (prerenal) but also by decreased renal blood flow to renal cellular fxnl units due to:
prolonged hypotension
hypoxemia
shock
sepsis
prolonged surgery (esp cardiac and major vascular)

35

How can ATN be secondary to toxins?

- may occur 5-10 days after exposure
- aminoglycosides (up to 25% of pts receiving thes drugs):
gentamicin, amikacin (Most nephrotoxic), streptomycin and tobramycin
- amphotericin B
- chemo
- acyclovir
- ethlyene glycol (anti-freeze)
- sulfonamides, cephalosporins

36

What is contrast nephropathy?

- form of ATN
- occurs 24-48 hrs post contrast exposure
- risk factors for development: DM, CKD, high contrast load, concurrent use of nephrotoxic drugs, age
- mechanism of injury unclear but likely involves:
direct toxicity of reactive O2 species (free radicals)
contrast induced diuresis
increased urinary viscosity
increased O2 consumption
imbalance of vasoconstriction vs vasodilation

37

How can we prevent contrast nephropathy?

- min amt of contrast used - talk to radiologist
- hydrate pre and post procedure with NS
- mucomyst (N-Acetylcysteine): 600 mg po BIDx 3 days starting day prior to procedure
- stop metformin (glucophage) the day of contrast load and for 48 hr post (can lead to lactic acidosis)
- Ask yourself: Do you really need this test? any alternatives?

38

Other causes of ATN?

- blood transfusion rxn, hemolytic anemia
- multiple myeloma
- uric acid
- myoglobin: muscle breakdown, when severe called rhabdomyolysis (CK greater than 16000), crush injuries, muscle necrosis from pressure pts in unconscious pts, seizures, cocaine, and ETOH

39

What is the FENa used for?

- useful for determining if the casue of AKI is prerenal or ATN
- prerenal if FENa is less than 1%
- intrinsic if FENa is greater than 2%

40

What are dark granular and epithelial casts indicators of?

- pure ATN

41

What are crystals an indicator of?

- crystalluric ARF

42

What are WBCs and WBC casts indicators of?

- acute interstitial nephritis

43

What are RBCs and RBC casts indicators of?

- proliferative/necrotizing glomerulonephritis

44

Management of AKI?

- tx underlying cause!!!
- maintain euvolemia
- manage electrolytes
- manage BP
- stop potentially nephrotoxic meds!!!!
- may need temporally dialysis

45

General work up of AKI?

- assess volume status
- UA: dipstick, microscopic exam, urine Na+, urine Cr
- CBC
- serum BUN and Creatinine (BMP)
- fractional excretion of NA+

46

What imaging studies do you want to do in intrinsic AKI?

- renal US
- bladder scan for post void residual
- CT or MRI
- renal bx in certain cases

47

What test is most impt noninvasive test in dx eval of pts with AKI?

- UA

48

Labs of prerenal AKI?

- urine Na is going to be less than 20
- BUN/Cr ratio will be more than 20:1
- FEna is less than 1

49

Labs of intrinsic AKI?

- Urine Na will be greater than 20
- BUN/Cr ratio less than 10:1, and FEna is greater than 2

50

Labs of postrenal AKI?

- urine Na will vary
- BUN/Cr will be nomral 10-20:1
- FEna will be variable